Workbook ENT Flashcards
Describe the innervation to the external ear.
- upper lateral surface
- lower lateral and medial
- superior medial
- external auditory meatus
- auticulotemporal V3
- greater auricular C3
- lesser occipital C2/3
- auricular branch of vagus
management of external ear laceration
closure of skin with sutures after adequate cleaning
clover any exposed cartilage
skin loss may require plastics input
management of ear bites
ascertain who bit the ear and work out the commensal organisms.
wound must be left open.
irrigation and antibiotics
management of pinna haematoma
disrupt the blood supply to the cartilage by stripping away the overlying perichondrium
this can lead to AVN and cauliflower ear deformity
urgent drainage and pressure dressing to prevent reaccumulation
tympanic membrane perforation
pain and possible conductive hearing loss
most heal by themselves- watch and wait with water precautions
if doesn’t heal at 6/12, may benefit from surgery (myringoplasty to repair TM if perforation is causing problems)
Haemotympanum
caused by trauma
associated with temporal bone fracture
conductive hearing loss
treated conservatively but follow up for residual hearing loss from damage to ossicles
otitis externa features
swimmers ear
bacterial or fungal inflammation of skin lining external canal
caused by regular skin commensals
painful ear discharge, itchy ear, hearing may be muffled
malignant otitis externa features
aggressive infection of external ear seen in diabetics and immunosuppressed individuals
infection spreads to bone
chronic ear discharge despite topical treatment, deep seated severe ear pain, cranial nerve palsies (CVII)
10% mortality
management of otitis external
topical gentamicin ear drops
swab discharge if resistant
micro suction of pus/debris?
severe infection may need with to keep ear open to deliver gentamicin
antifungals if fungal
malignant OM requires IV abs with extended topical abs to eradicate infection
middle ear epithelium
respiratory epithelium- pseudo stratified columnar
continuation of respiratory epithelium
same organisms cause infections- strep pneumonia, haemophilia influenza, moraxella
Features of AOM
ear pain caused by increased pressure in tympanic cavity (children may pull their ears)
discharge from tympanic membrane rupture
fever
management of AOM
conservative- analgesia
medical- severe cases require abs
recurrent- may require surgery (grommet)
forms of chronic otitis media
- active mucosal - discharge from middle ear through TM perforation
- active squamous - cholesteatoma
- inactive mucosal - TM perforation byt no infection/discharge
- inactive squamous - retraction pocket
how does mucosal chronic OM develop?
from an episode of AOM after rupturing the TM there is failure to heal.
how does active squamous OM develop?
keratinised squamous cells are introduced into the middle ear and form a retraction pocket or a perforation
what is active chronic OM associated with?
chronic ear discharge
conductive hearing loss
complications- spread of disease into temporal bone or intracranially
management of chronic OM
cholesteatoma- surgery to clear cholesteatoma and any affected mastoid bone (mastoidectomy)
mucosal disease- topical abx and aural toilet
what if you are not sure if cholesteatoma is present in a chronically discharging ear?
treat medically first, then surgically if doesn’t settle. if in surgery no cholesteatoma is discovered, repair perforation and ensure good ventilation
risks of mastoid surgery
facial nerve palsy altered taste from chords tympani palsy CSF leak tinnitus vertigo complete hearing loss in that ear
OM with effusion (glue ear) features
fluid in middle ear with intact tympanic membrane
related to euschasian tube dysfunction
common in children
in adults, exclude tumour causing obstruction to ET drainage
not painful, but cam before infected (AOM) which is painful
middle ear effusion on otoscope and conductive hearing loss (speech delay, school problems)
how might you investigate OM with effusion?
- tymponogram - flat type B trade with normal canal volume
2. pure tone audiometry- conductive hearing loss
how is OM with effusion managed?
conservative- 3 months
hearing aid
surgery if prolonged and causing significant problems (grommets, ?adenoidectomy)
what is otosclerosis?
disease of ossicles where mature bone is replaced by woven bone
symptoms develop as stapes becomes fixed to oval windows
can be environmental or genetic (autosomal dominant)
epidemiology of otosclerosis
1-2% of population have it and have symptoms from it
85% will have bilateral disease
F:M 2:1
features of otosclerosis
progressive hearing loss
?tinnitus
improved hearing in noisy surroundings at early stages
?family history
examination findings in otosclerosis
usually normal examination
rarely schwartze’s sign seen- pink hue to TM
investigation findings in otosclerosis
- tymponogram- normal type A trace
2. pure tone audiogram- conductive hearing loss, charicteristic Carhart notch at 2kHz
management of otosclerosis
hearing aid
stapedectomy
where is the inner ear?
petrous part of temporal bone
what does the inner ear consist of?
labyrinth of canals: vestibule and semicircular canals, cochlea
outline the structure of the labyrinth
membranous labyrinth is filled with endolymph (similar to intracellular fluid). this is surrounded by perilymph (similar to CSF), and contained within the bony labyrinth.
perilymphatic system communicated with subarachnoid space and CSF via the cholerar aqueduct
how is the cchlea (responsible for perception of hearing) different from the rest of the labyrinthine system?
- 2.5 turns around bony core (modiolus)
- stapes articulates with oval window, moves perilymph, pressure changes are compensated by round window
- vibrations transmitted through the endolymph to the tectorial membrane
- movement of tectorial membrane causes movement of hair cells, subsequent depolarisation of neuronal fibres and perception of sound
- information transmitted via cochlear nerve
where in the cochlea are different sounds detected?
low frequency- apex
high frequency- base of cochlea
what makes up the vestibular system?
semicircular canals (three, at 90 degrees to each other)
utricle
saccule
functions of vestibular system
Utricle- hairs point up to detect horizontal movement
saccule- hairs on side to detect vertical movement
semicircular canals- detect rotatory movement
what contributes to good balance?
vestibular system
proprioception
vision
what is vertigo?
hallucination of movement
associated with vestibular system problems
central causes of vertigo
stroke migrane neoplasm demyelination e.g. MS Drugs
peripheral causes of vertigo
BPPV
Menieres
Vestibular Neuronitis
BPPV
- features
- pathophysiology
- vertigo with head movements lasting seconds-minutes, very distressing
- otoliths (crystals) in semicircular canals (usually posterior) cause abnormal stimulation of hair cells
how is BPPV
- diagnosed
- treated
- Dix-Hallpike test
2. Epley manoeuvre
pathophysiology of Menieres disease
endolymphatic hydrops (increased fluid in endolympthatic compartment)
clinical features of Menieres
tinnitus in affected ear
episodic vertigo lasting minutes- hours with N&V
fluctuating sensorineural hearing loss which over time becomes permanent
aural fullness
investigations for sudden onset sensorineural hearing loss
pure tone audiogram
MRI scan to exclude lesion along central auditory pathway eg acoustic neuroma
management of sudden onset sensorineural hearing loss
steroids - usually oral, can be injected into middle ear
antivirals
rarely hyperbaric oxygen or carbogen
which hearing loss requires urgent treatment?
sudden onset sensorineural
which tuning forks are used?
256 or 512Hz
Weber test
on forehead
localises to ear with conductive hearing loss/without sensorineural hearing loss
(because in conductive hearing loss, background noise is cancelled out and bone conduction is normal)
Rinne test
placed on mastoid bone until can’t hear. then, placed against external auditory meatus.
conducted to cochlea via temporal bone
can still hear it = positive result = sensorineural and normal (AC>BC)
can’t hear it= negative result= conductive hearing loss (BC>AC)
Pure tone audiogram
tests hearing thresh points at different frequencies
can be used from age 4
quietest tone which can be reliably heard by each ear at different frequencies is plotted
air conduction and bone conduction thresholds tested
pure tone audigraph
frequency in Hz on x axis
descend on y axis in decibels (the quieter the noise, the higher the line and better hearing. anything above 20dB is normal)
Menieres disease course
initially- well between attacks
progresses
feel generally unsteady due to reduced vestibular Winston and progressive sensorineural hearing loss
disease often burns out- no more acute vertigo, but reduced heating and generally unbalanced
is the vestibular system of the other ear is working well, this can compensate for bad ear
dietary management of Menieres
reduce salt, chocolate, alcohol, caffeine, Chinese food
medical management of Menieres
Thiazide diuretic
Betahistine
vestibular sedatives eg prochlorperazine for acute attacks
surgical management options for Menieres
Grommets dexamethasone middle ear injection Endolymphatic sac decompression vestibular destruction using middle ear injection of gentamicin surgical labyrinthectomy (rare)
What is vestibular neuritis
inflammation of middle ear
severe incapacitating vertigo lasting several days with N&V
during attack- horizontal nystagmus but otherise normal neurological examination
treatment of vestibular neuritis
symptomatic:
vestibular sedatives during acute episode
IV fluids
prognosis of vestibular neuritis
often long term vestibular deficit after the acute episode which can lead to generalised unsteadiness for a number of weeks
management of long term complications of vestibular neuritis
if patients are suffering from a long term vestibular dysfunction in one ear, may be helped by vestibular rehabilitation exercises such as the Cawthorne-Cooksey exercises. after the acute attacks, patients should not take vestibular suppressants as this delays recovery.
sudden onset sensorineural hearing loss
otological emergency
prognosis for sudden onset sensorineural hearing loss
1/3 recovery to normal
1/3 some recovery
1/3 no recovery
how is bone conduction tested during PTA
tone played through conductor placed over mastoid bone.
sound passes through bone straight into cochlea, bypassing conductive hearing system, so it approximates sensorineural hearing.
some sound is conducted to the other ear, so if there are any disprecancies between two ears, the other ear will need to be masked.
features of conductive hearing loss
impedance to hearing in middle or external ear
eg wax, OM with effusion
PTA will show normal BC and reduced AC (an air bone gap)
features of sensorineural hearing loss
problem in cochlea-auditory cortex of the brain
asymmetrical sensorineural hearing loss should be investigated with an MRI scan looking for lesions along the pathway eg acoustic neuroma (vestibular schwannoma)
PTA will have reduced AB and reduced BC- no air bone gap
old age hearing loss
bilateral
sensorineural
presbycusis
(may also be components of conductive)
tymponogram
simple test which measures compliance of TM and gives information about TM, middle ear and ET function.
probe is inserted into external ear canal
can be done at any age, takes few seconds, and requires minimal cooperation from patient
reading from tymponogram
compliance in ml (y axis) vs pressure (x axis in daPascals)
compliance of TM measured with varying amounts of pressure in external canal which is sealed by probe.
compliance peaks when pressure in canal equals that of middle ear
type A tymponogram trace
normal result
peak at 0kPa
type B tymponogram trace
flat tracing
suggests middle ear effusion or perforation
by look at the canal volume reading on the side of the tymponogram you can differentiate between effusion and perforation. effusion has a normal canal volume (1ml in adults) whereas in perforation the volume is much larger
type C tymponogram trace
peak of tracing has a negative pressure
suggests ET dysfunction
Little’s area
also known as Kiesselbach’s plexus
highly vascular area on nasal septum
receives contribution from branches of external carotid and internal carotid arteries
Epistaxis- what is it
bleeding from nose
local causes of epistaxis
idiopathic 85% traumatic iatrogenic foreign body inflammatory- rhinitis, polyps neoplasm
systemic causes of epistaxis
HTN
coagulopathies
vasculopathies
hereditary haemorrhage telangiectasia/osler-weber-rendu disease
management of epistaxis
ABC pinch soft part of nose head forward spit out blood cautery (silver nitrate or bipolar diathermy) nasal packing if cautery fails
detail on epistaxis cautery
silver nitrate or bipolar diathermy
if anterior bleed- with anterior rhinoscopy
if posterior bleed- with rigid endoscope
topical adrenaline may help control bleeding
surgical management of epistaxis
if nasal packing fails, vessels can be surgically ligated or radiological embossed:
sphenopalatine
anterior ethmoid (cannot be embossed because it comes form international carotid)
external carotid
complications of nasal fracture
septal haematoma
CSF leak associated with skull base fracture
management of nasal trauma
ABC
examine for septal haematoma
no XR required
consider manipulation under anaesthetic within 2 weeks of injury (LA/GA)
lamina papyracea
forms medial wall of orbit
what drains into these structures?
- sphenoid-ethmoidal rescues
- superior meatus
- middle meatus
- inferior meatus
- sphenoid sinus
- posterior ethmoid cels
- frontal, maxillary and anterior ethmoid cells
- nasolacrimal duct
complications of sinus surgery
- damage to orbit- lies lateral to ethmoid sinus and superior to maxillary sinus (severe cases can cause loss of sight)
- anterior skull base- lies just above the sphenoid and ethmoid sinuses and can be breached during surgery which can cause CSF leak and brain damage
complications of rhino sinusitis
- can spread to orbit to cause peri orbital sinusitis which can be sight threatening
- from frontal sinus can spread intracranially causing meningitis and intracranial abscesses
define rhino sinusitis
inflammation of nose and paranasal sinuses characterised by two or more symptoms, one of which could be:
- nasal blockage/obstruction/congestion/discharge
- anterior/posterior postnasal drip
- facial pain/pressure
- reduced sense of smell
other features of rhinosinusitis
- endoscopic signs of polyps, mucopurulent discharge or oedema in middle meatus
- CT changes- mucosal changed within the osteomatal complex or sinuses
how is rhino sinusitis classified?
Acute: <12/52, complete resolution of symptoms. viral or on viral
Chronic: 12/52, without complete resolution of symptoms
with or without polyps
ARS
Viral ARS (common cold) is usually caused by rhinovirus or influenza virus with resolution within 5 days
non viral ARS is considered if >5/7, usually bacterial: H influenzae, Moraxella catarrhalis.
allergy and ciliary impairment predispose to ARS
management of ARS
analgesia
nasal decongestant
if >5/7, consider nasal steroids and oral abs
CRS predisposing factors
Allergy, Infection, Ciliary impairment (CF, nasal polyps), Anatomical (septal deviation, abnormal unicante process leading to narrow infundibulum and occlusion of osteomeatal couples), immunocompromised, aspirin hypersensitivity, Atmospheric irritants (smoking, dust, fumes), hormonal (pregnancy, hypothyroidism), trauma (oroantral fistula, nasal sinus fracture), foreign body in nose or sinus, swimming
CRS in pregnancy
oestrogen and progesterone increase mucosal vascularity and predispose to CRS
Nasal polyps
inflammatory mass
normally bilateral
biopsy if unilateral or worrying signs or findings
investigating CRS
skin prick if allergy suspected CT sinuses (if surgery is planned, if atypical features- not good for diagnosis as many patients will have sinus changes even if asymptomatic)
management of CRS
conservative- avoid allergens, nasal douching
medical- antihistamines, topical nasal steroid, one week oral steroids if severe, oral antibiotics
surgical- nasal polypectomy (very high rate of recurrence), functional endoscopic sinus surgery to improve drainage/ventilation, septoplasty, reduction of inferior turbinates
what is allergic rhinitis
an IgE mediated type 1 hypersensitivity reaction in the mucus membranes of nasal airways. affects 30% western population. associated with asthma. seasonal or perennial. commonest allergens: pollens, moulds, house dust mites, animal epithelia
how is allergic rhinitis classified?
allergic rhinitis according to its impact on asthma (ARIA) and other health issues. based on duration and severity
duration of allergic rhinitis.
intermitent <4 days a week, less than 4 weeks
persistent >4 days a week, more than 4 weeks
severity of symptoms of allergic rhinitis
mild- normal daily activities and sleep
moderate to severe- impairment of daily activities and sleep, troublesome symptoms
pathophysiology of allergic rhinitis
synthesis and release of arachidonic acid metabolites (prostaglandin D and leukotrienes) and mast cell degranulation. in turn increased capillary permeability leading to congestion, odedema, rhinorrhoes, sneezing and irritation
investigations for allergic rhinitis
SPT for specific antigen
RAST blood test if SPT not possible
management of allergic rhinitis
conservative - allergen avoidance, nasal douching
medical- antihistamines, topical nasal steroids
immunotherapy
how does periorbital sinusitis develop?
from direst spread of pus from the ethmoid sinus, or from thrombophlebitis of mucosal vessels in any of the sinuses
symptoms of periorbital sinusitis
pain followed by oedema of the eyelids
is orbital abscess develops- eye will become proposed and eye movements will be reduced.
risk of blindness as a result of tension and septic necrosis of the optic nerve.
colour blindness is an early sign
investigating periorbital sinusitis
CT scan will confirm the collection and the extent of the disease
treatment of periorbital sinusitis
IV abs
nasal decongestants
urgent surgical drainage if abscess
boundaries of anterior triangle of the neck
- medial
- lateral
- superior
- midline of neck
- anterior boarder of SCM
- lower boarder of the mandible
posterior triangle of neck boundaries
- anterior
- posterior
- base
- posterior boarder of SCM
- anterior edge of trapezius
- middle third of clavicle
where may a retropharyngeal abscess form?
anterior to the prevertebral fascia, behind the pharynx
is the retropharyngeal space. extends from base of skull to mediastinum.
clinical features of a retropharyngeal abscess
young child after URTI
neck held rigid and upright with reluctance to move
systematically unwell
airway compromise
dysphagia/odynophagia
widening of retropharyngeal space on lateral X ray
associated mortality due to airway problems and mediastinitis
investigations for a retropharyngeal abscess
CT neck
management of a retropharyngeal abscess
secure airway if any concerns
IV abs
surgery- I&D
what is Ludwigs angina
infection of the space between the floor of the mouth and mylohyoid, commonly associated with dental infection
clinical features of Ludwigs angina
swelling of the floor of the mouth painful mouth protruding tongue airway compromise drooling
investigations for Ludwig’s andgina
CT neck
OPG
management of Ludwigs angina
secure airway if concerns
IV abs
surgery to drain any collection
where is a parapharyngeal abscess?
posteriolateral to oropharynx and nasopharynx which is divided by the styloid process.
how does a parapharyngeal abscess present?
similar to peritonsillar abscess or quinsy
febrile illness, odynophagia, trismus, reduced neck movement, swelling in the neck and around the upper part of the SCM.
parapharyngeal space contains the carotid sheath- risk of severe complications in this area
management of parapharyngeal abscess
secure airway if concerned
IV abs
surgical drainage
epiglottitis causes
haemophilus influenza
incidence reduced by HIB vaccine
presentation of epiglottis
stridor
drooling
pyrexia
rapidly progressive
management of epiglottis
secure the airway- do not examine keep calm if possible, take child to theatre and intubate by paediatric anaesthetist with an ENT surgeon on standby to do a surgical airway if intubation is not possible. if transfer to theatre not safe, intubate in A&E IV abs (normally respond within couple days and then extubated)
Neck lumps where may these be found? 1. parotid neoplasm 2. jugulodigastric 3. submandibular gland 4. carotid body tumour or aneurysm
- anterior to ear
- angle of mandible
- inferior boarder of mandible
- at bifurcation of common carotid artery
neck lumps- where may these be found?
- thyroglossal cyst
- branchial cyst
- thyroid nodule
- Virchows node
- in midline between hyoid bone and thyroid gland
- anterior boarder of SCM
- at level of thyroid
- supraclavicular dossa node may represent metastasis
where is the oral cavity?
lips - posterior soft palate
whee is the nasopharynx?
base of skull to level of soft palate
contains adenoids and ET opening
where is the oropharynx?
from soft palate to superior boarder of epiglottis
contains palatine tonsils and anterior and posterior tonsillar pillars
where is the hypotharynx?
from superior boarder of epiglottis to inferior boarder of cricoid cartilage, posterior to the larynx
muscles of pharynx
a circular layer formed by superior, middle and inferior constrictors, and the cricopharynxgeus
Killian’s dehiscence
area deficient in muscle between the inferior constrictor and the cricopharyngeous
site of pharyngeal pouches
how fo pharyngeal pouches present?
dysphagia, delayed regurgitation of food and sometimes recurrent chest infections due to aspirated food
which muscles cause elevation and depression of pharynx?
stylopharyngeous
salpingopharyngeous
palatopharyngeous
what is snoring a sign of?
partial obstruction of the upper airway during sleep (nose-larynx)
what is the pathophysiology of OSA?
complete obstruction of upper airway during sleep requires patient to wake up and reposition to open up the airway. apnoeas result in poor nights sleep and strain on caridovascular system.
main causes of OSA
obesity in adults
adenotonsillar hypertrophy in children
investigations to consider in OSA
BMU TFT for hypo CXR for obstructive lung disease ECG for signs of RV failure sleep study
management of OSA
weight loss
CPAP
?mandubular repositioning devices
?adenotonsilectomy in children (rare in adults)
bacterial causes of tonsillitis
B haemolytic strep staphylococci strep pneumonia haemophilus influenza E coli
viral causes of tonsillitis
adenovirus
rhinovirus
enterovirus
EBV
amoxicillin in tonsilitis
should be avoided
will cause maculopapular rash in EBV
EBV advice
avoid contact sport for 2-3 months due to hepatosplenomegaly
quinsy
peritonsillar abscess
sore throat localised to one side and a ‘hot potato’ voice
amendable to drainage under LA
histopathology of H&N cancers
90% are SCC
which ethnicity has a higher risk of nasopharyngeal malignancy?
Chinese
when is histology/cytology of neck lumps not required?
proven H&N SCC (assume any LN are due to this- CT)
why should you do FNA before core biopsy
core biopsy can lead to tumour seeding therefor FNA first, exclude SCC, core biopsy to diagnose TB or lymphoma
what is a goitre?
an enlarged thyroid gland
what is a thyroid nodule?
an abnormal mass in the thyroid
investigation of thyroid nodules
check that they are not functioning leading to hyperthyroidism and that they are not neoplastic
complications of large goitres?
can cause compression leading to airway obstruction and dysphagia
blood supply and drainage to thyroid gland
supply- superior and inferior thyroid arteries
drainage- superior, middle and inferior thyroid veins
where is the RLN at the thyroid?
intimately associates with the thyroid glad: run in the tracheooesophygeal groove therefore at risk during surgery
RLN function
supply the muscles of the larynx except cricothyroid and sensation below vocal cords
injury of RLN
vocal cord palsy- hoarseness, upper airway obstruction in both damaged
assessment of thyroid nodules
FNA
if there is any diagnostic doubt, hemithyroidectomy for definitive histology
lumpectomies are not done because if it is malignant the margins would likely not be enough and scarring would make further surgeries difficult
FNA are not accurate for differentiating follicular carcinoma from follicular adenoma and in these cases hemithyroidectomy should be done
non-neoplastic thyroid nodules
single nodule- colloid, cystic
multi nodular goitre- common, typical features on USS and no need for FNA. any dominant nodule however should have FNA
thyroid neoplasms
benign- usually follicular adenoma
malignant:
papillary adenocarcinoma (70%, younger pt or history of neck radiation)
follicular carcinoma- 20% (preponderance to met to bones and lung)
rare thyroid malignant neoplasms
medullary carcinoma 5%- neoplasm of calcitonin regulating C cells, frequently seen in MEN syndromes
anaplastic carcinoma 5%- typically in older patients, poor prognosis (weeks to months)
management of non neoplastic thyroid nodules
usually conservative unless diagnostic uncertainty
surgery: for compressive symptoms, cosmoses or patient preference
(hemithyroidectomy is best because total thyroidectomy requires lifelong thyroxine)
management of neoplastic thyroid nodules
adenomas require no further treatment after diagnostic hemithyroidectomy
carcinoma- surgery (total for papillary, follicular and medullary, anaplastic disease is usually too advanced for surgery)
radio iodine therapy for papillary and follicular after surgery
complications of thyroid surgery
post op haemorrhage
airway obstruction (secondary to haemorrhage, secondary to bilateral vocal cord palsy)
vocal cord palsy
hypocalcaemia
parotid gland anatomy
serous salivary gland located anterior to pinna and lateral to the ramps of the mandible
split into deep and superficial lobes by the facial nerve which passes through it
majority is superficial
facial nerve palsy is a serious complication of parotid cancer or surgery
parotid duct anatomy
opens opposite the second upper molar tooth after piercing the buccinator muscle and buccal mucosa
salivary gland neoplasms
80% in parotid
80% of parotid neoplasms are benign
80% of benign parotid neoplasms are pleomorphic adenomas
salivary gland infections
9X more common in submandibular than parotid
submandibular gland anatomy
located inferior to the mandible and superior to the digastric
its duct opens into the mouth close to the frenulum of the tongue
hypoglossal and lingual nerves run medial to the gland and are at risk during surgery
produces mixed mucous and serous secretions
sublingual gland secretions
entirely mucous
located at the floor of the mouth
submandibular gland neoplasms
50% are malignant
sublingual gland neoplasms
80% are malignant
submandibular abscesses
can follow sialolithiasis or sialadenitis
acute sialadenitis
can be viral or bacteria
bacterial usually staphylococcal (dehydrated or immunocompromised)
viral: paramyxovirus (mumps), coxsackievirus, echovirus, HIV
chronic sialadenitis
rare, seen in TB, sarcoidosis, HIV and syphilis
sialolithiasis
stones in salivary duct
cause obstruction and subsequently lead to pain and swelling which is worse during meals
9X more common in submandibular than parotid
investigations in suspected sialolithiasis
USS
or sialogram
management of sialolithiasis
most settle with conservative- analgesic, hydration, sialogogues
endoscopy
radiological removal
surgery (remove palpable stones or salivary gland)
complications of sialolithiasis
sialadenitis
abscess formation
Sjorgens syndrome features
Autoimmune disease causing lymphocytic infiltration into ductal tissue of secretory glands dry eyes dry mouth enlarged salivary gland increased lymphoma risk
causes of Sjorgens
primary- Xerostomia and Xerophthalmia without connective tissue abnormality
secondary- with connective tissue disease, eg rheumatoid arthritis
diagnosis of sjorgens
history, examination, some specific antibodies, biopsy of minor salivary glands on the inner lip
